The brain is a massive network of electrically active cells (neurons) that communicate with each other by synaptic transmission at specialized intercellular junctions called synapses. Ionotropic glutamate receptors (iGluRs) are the major mediators of excitatory synaptic transmission in the central nervous system (CNS). The N-methyl-D-aspartate subtype of glutamate receptor (NMDAR) has attracted particular interest because of its unique role in synaptic plasticity, memory formation and disease. Excessive activation of NMDARs has been associated with neuronal cell injury and death in hypoxic-ischemic brain injury, trauma and epilepsy, and several degenerative neurological disorders such as Huntington’s disease, amyotrophic lateral sclerosis, HIV dementia, Alzheimer’s disease and Parkinson’s disease. Dr. Jin’s research focuses on elucidating the molecular basis underlying NMDAR regulation and functional plasticity using a combination of biochemical, biophysical, and electrophysiological approaches. These studies will facilitate the design and improvement of therapeutic agents for the treatment of psychological and neurological disorders. A second area of research concerns the structure and function of botulinum neurotoxins (BoNTs), which are among the most poisonous substances known to man. BoNTs therefore represent a major bioterrorist threat. Paradoxically, BoNT-containing medicines and cosmetics, such as Botox® and Dysport®, have been used with great success in clinic. Both the toxic and therapeutic functions of BoNTs indeed rely on a common mechanism to enter neurons, cleave proteins that mediate exocytosis of key neurotransmitters, and subsequently paralyze the affected muscles. The Jin laboratory is attempting to understand the molecular mechanisms underlying the BoNT-host interplay during the course of intoxication. Specifically, Dr. Jin and his colleagues are interested in two major questions: (1) How does BoNT survive the harsh environment (low pH, protease-rich) of the gastrointestinal tract and penetrate gut epithelial cells to reach the general circulation? (2) How does BoNT recognize and invade nerve cells at neuromuscular junctions? A better understanding of these fundamental questions will guide the development of effective anti-BoNT strategies, will help improve clinical efficacy of BoNT-containing drugs, and will suggest novel applications for BoNT.